Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0016382 (flushing)
 6,387 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Donor exposure can be strikingly reduced for patients with classical hemophilia A and von Willebrand's disease when large volumes of potent cryoprecipitated AHF are prepared from donors following DDAVP (1-deamino-8-D-arginine vasopressin) stimulation and automated plasmapheresis--a procedure called "plasma exchange donation." Although this procedure has been reported to be relatively safe for donors, data are limited. Accordingly, we studied 20 donors during 48 procedures using DDAVP (0.3 micrograms/kg IV) followed by 2-3 L plasma collection. Replacement fluid for each initial plasma exchange donation was plasma protein fraction; autologous cryoprecipitate-poor plasma was used for subsequent procedures. Mild reactions, particularly facial flushing, were noted in all 48 procedures. No procedure was discontinued, but four were modified due to either an increased pulse rate (> or = 20/min from baseline) or a fall in systolic or diastolic blood pressure (> or = 20 mm Hg from baseline). No donor was deferred or withdrew from the program. Based on our modest experience, DDAVP stimulated plasma exchange donation appears to be a safe and effective method for collecting large quantities of plasma from which potent cryoprecipitated AHF can be prepared.
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PMID:Donor reactions during DDAVP-stimulated plasmapheresis. 142 92

1. The mechanism of the flushing, hypotension and tachycardia associated with i.v. administration of desGlyd(CH2)5D-Tyr(Et)VAVP (SK&F 101926; 25 micrograms kg-1) and the selective V2 antidiuretic agonist, desamino-8-D-arginine vasopressin (dDAVP; 3 micrograms kg-1) was studied in ketamine-anaesthetized rhesus monkeys. 2. The flushing associated with SK&F 101926 was reduced by pretreatment with a mast cell stabilizer and by repeated administration of peptide (within 2-4 weeks). A similar desensitization to dDAVP-associated flushing was observed on repeated administration. 3. Treatment with dDAVP also resulted in reduced SK&F 101926-associated flushing. 4. The hypotension associated with SK&F 101926 was not affected by pretreatment with a mast cell stabilizer. A similar degree of hypotension was observed with repeated administration of either SK&F 101926 or dDAVP. 5. The tachycardia associated with SK&F 101926 was reduced by pretreatment with a mast cell stabilizer or repeated administration of SK&F 101926. Repeated administration of dDAVP, however, resulted in an enhanced tachycardia. 6. Indomethacin (5 mg kg-1 i.v.) did not alter the flushing or the hypotension associated with the administration of either SK&F 101926 or dDAVP, but resulted in an enhanced tachycardia to SK&F 101926. 7. Administration of a selective V1 vasopressor antagonist did not result in flushing, hypotension or tachycardia. 8. It was concluded that the flushing response to vasopressin-like peptides in rhesus monkeys may be due to an action on mast cells, whereas the haemodynamic responses are not, but probably involve direct vasodilator actions.
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PMID:Flushing and haemodynamic responses to vasopressin peptides in the rhesus monkey. 317 11

The mechanisms of the cardiovascular and renin responses to vasoactive intestinal polypeptide (VIP) are unclear. Rabbit studies suggest that VIP-induced tachycardia is largely beta-adrenoceptor mediated, but that the renin response may be partially prostaglandin-dependent. To examine the relative importance of prostaglandins and reflex sympathetic activation in the haemodynamic and renin responses to VIP infusion in man, we completed two randomised single-blind crossover studies in two groups of six healthy male volunteers (aged 24-35 years). We recorded the effects of indomethacin and propranolol pretreatment on VIP-related changes in heart rate (HR), blood pressure (BP), forearm vascular resistance (FVR), plasma renin activity (PRA), plasma noradrenaline (PNA) and plasma arginine vasopressin (AVP) concentrations. Intravenous VIP (calculated dose: 6 pmol kg-1 min-1) produced cutaneous flushing, increased HR and PRA, decreased FVR, but did not alter mean arterial BP or AVP levels. Indomethacin (375 mg over 3 days) lowered basal PRA and propranolol (circa 40 mg i.v. over 60 min) decreased resting HR and increased FVR. Although indomethacin and propranolol reduced the absolute rise in PRA and HR, respectively, during VIP infusion, the percentage changes were no different from control. Neither drug altered the flush response to VIP and propranolol did not affect the fall in FVR. We conclude that the measured cardiovascular responses to VIP infusion in man are probably direct and do not involve a significant contribution from reflex sympathetic stimulation, nor prostaglandin release.
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PMID:Effects of indomethacin and (+/-)-propranolol on the cardiovascular and renin responses to vasoactive intestinal polypeptide (VIP) infusion in man. 329 24

Between 1981 and 1986, we evaluated 59 patients who presented with isolated prolongation of bleeding time with normal platelet counts, platelet aggregation and coagulation parameters (including von Willebrand's factor), and without evidence of liver or kidney disease, or exposure to anti-platelet agents. These patients, termed as vascular fragility syndrome (VFS), were analyzed to further characterize their bleeding patterns. The pattern of bleeding manifestations was similar to that of patients with platelet dysfunction, such as mucocutaneous bleeding or excessive post-operative bleeding. In 16 patients, desmopressin (1-desamino-8-d-arginine vasopressin, DDAVP) was infused to control active bleeding or as a part of pre-surgical evaluation. Bleeding time improved (pre-DDAVP bleeding time 15.3 +/- 3.4 min, mean +/- S.D.; post-DDAVP bleeding time 10.7 +/- 3.9 min; p less than 0.01) within 30 minutes following the DDAVP infusion with either satisfactory arrest of acute bleeding or good control of subsequent hemostasis with surgery. Side effects with DDAVP were transient and minor, i.e. facial flushing, or conjunctival erythema. These findings indicate that VFS with isolated prolongation of bleeding time is a frequently encountered bleeding disorder and that DDAVP is effective in achieving hemostasis for the management of acute bleeding and may be useful prior to surgical procedures.
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PMID:Patients with prolonged bleeding time of undefined etiology, and their response to desmopressin. 338 95

Hormonal and cardiovascular responses to 1-desamino-8-D-arginine vasopressin (DDAVP) were investigated in six normal adult volunteers. After overnight fluid deprivation, an intravenous injection of either DDAVP (0.4 microgram/kg) or the same volume of normal saline was administered. One hour later an intravenous infusion of hypertonic saline was commenced and continued over two hours. Five minutes following the DDAVP injection, facial flushing, a fall in diastolic blood pressure by an average of 13% and a rise in pulse rate by an average of 18% were observed. There was a significant increase in plasma renin activity and plasma cortisol concentration, but no significant changes were observed in plasma concentrations of LH, FSH, TSH, prolactin or GH. Following osmotic stimulation by hypertonic saline plasma AVP rose to the same extent in both the DDAVP and control studies. DDAVP (0.4 microgram/kg) was also administered to five subjects with cranial diabetes insipidus. Again facial flushing, increased facial temperature, a fall in diastolic pressure and a rise in heart rate were all observed, suggesting that DDAVP exerts its cardiovascular actions by a mechanism other than antagonism of circulating endogenous AVP.
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PMID:Hormonal and cardiovascular responses to DDAVP in man. 351 5

Des-amino-D-arginine vasopressin (DDAVP) stimulates the release of factor VIII and plasminogen activator from the vascular endothelium. An infusion of exogenous factor VIII given to haemophiliacs causes an increase in platelet activation. This activation does not occur after stimulating a rise in the patient's own factor VIII level caused by DDAVP infusion. We hypothesised therefore that DDAVP could also cause the endothelial release of prostacyclin (PGI2), a potent anti-platelet agent which would counteract the aggregating effect of factor VIII. To examine this possibility we studied the effect of DDAVP on prostacyclin release, as measured by its stable metabolite 6-oxo-PGF1 alpha, in vitro and in vivo. Rabbit aortic rings were incubated with different concentrations of DDAVP using saline as control. The supernatant was assayed for 6-oxo-PGF1 alpha by radioimmunoassay. All concentrations of DDAVP gave a significant release of 6-oxo-PGF1 alpha. Vasopressin was much less potent. When DDAVP was infused into haemophilic patients there was a significant increase in circulating 6-oxo-PGF1 alpha levels immediately after the infusion. The facial flushing observed as a side-effect of DDAVP could therefore be prostacyclin-mediated. We confirmed this by abolishing the DDAVP induced flushing seen in normal subjects by prior treatment with aspirin which inhibits PGI2 formation.
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PMID:DDAVP stimulates prostacyclin production. 680 93

The use of 1 deamino-8-D-arginine vasopressin (DDVAP), is reported in seven patients with von Willebrand's disease and mild haemophilia undergoing elective surgery. There were no haemorrhagic complications, and both the quality of the clot formed and the rate of healing appeared entirely normal in all patients. No patient received blood products. Local burning pain due to paravenous leakage at the infusion site in a single patient, and transient facial flushing in another were the only side effects encountered. In addition to the anticipated rise in F.VIII:C and F.VIIIR:Ag, shortening of the bleeding time was observed in all five patients with von Willebrand's disease receiving DDAVP. Three additional patients who received intranasal DDAVP showed an inconsistent response in the laboratory parameters measured.
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PMID:Clinical experience with arginine vasopressin (DDAVP) in von Willebrand's disease and mild haemophilia. 697 Sep 7

Three patients with autosomal-recessive nephrogenic diabetes insipidus (NDI), homozygous for mutations in the aquaporin 2 gene (AQP2), were tested for their fibrinolytic and hemodynamic responses to intravenous administration of 1-desamino-8-D-arginine vasopressin (DDAVP). They all showed an increase of tissue-type plasminogen activator antigen, facial flushing, an increase of heart rate and a decrease of diastolic blood pressure. These results confirm the hypothesis that NDI patients with an AQP2 defect can be discriminated from NDI patients with a vasopressin type 2 receptor defect by their normal extrarenal responses to DDAVP.
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PMID:Normal fibrinolytic responses to 1-desamino-8-D-arginine vasopressin in patients with nephrogenic diabetes insipidus caused by mutations in the aquaporin 2 gene. 873 Apr 18

We describe a case of a novel mutant vasopressin 2 receptor (V2R)-dependent nephrogenic diabetes insipidus (NDI) with bilateral non-obstructive hydronephrosis in a middle aged man. This could be distinguished from aquaporin 2 (AQP2)-dependent NDI by the response of factor VIII and von Willebrand factor (vWF) to 1-deamino-8-D-arginine vasopressin (DDAVP) administration. A 47-year-old man was admitted to hospital because of polyuria, which had been present from infancy and was suspected of causing non-obstructive hydronephrosis. His mother's father, the older brother of his mother and his second daughter also all had polyuria. Sodium concentration, osmolality and vasopressin in blood were high, while sodium concentration and osmolality in urine were low. There were no changes in urine osmolality, factor VIII and vWF in response to DDAVP infusion. Neither was heart rate, diastolic blood pressure nor facial flushing affected. These findings suggested this case was V2R-dependent NDI rather than AQP2-dependent NDI. Molecular genetic analysis demonstrated that the patient had a V2R missense mutation involving a substitution of cysteine for arginine at position 104 (R104C) located in the first extracellular loop of the V2R. It was also found that the patient's mother and his second daughter were heterozygous for this R104C mutation.
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PMID:A case of a novel mutant vasopressin receptor-dependent nephrogenic diabetes insipidus with bilateral non-obstructive hydronephrosis in a middle aged man: differentiation from aquaporin-dependent nephrogenic diabetes insipidus by response of factor VII and von Willebrand factor to 1-diamino-8-arginine vasopressin administration. 1470 55